DETECTION OF TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-1-BETA IN THE RHEUMATOID OSTEOARTHRITIC CARTILAGE-PANNUS JUNCTION BY IMMUNOHISTOCHEMICAL METHODS

During inflammation the rheumatoid synovial membrane is invaded by a n umber of different cell types. When activated most of these cells prod uce cytokines including tumor necrosis factor alpha (TNFalpha) and int erleukin-1 beta (IL-1 beta). These cytokines are believed to stimulate production of degradative enzymes and disturb the equilibrium between such enzymes and their inhibitors resulting in tissue damage. In this study we investigated the localisation of TNFalpha and IL-1 beta at t he cartilage-pannus junction (CPJ). Here, cytokines are well placed to influence the integrity of articular cartilage. Tissue was derived fr om advanced rheumatoid (RA) and, as a comparison, osteoarthritic (OA) joints at the time of replacement surgery (arthroplasty). Antibody sta ining of fixed serial sections of tissue localised cells that were ass ociated with IL-1 beta and TNFalpha. Cell markers for macrophages and endothelial cells were included to provide positive identification of the cytokine-associated cells. Anaylsis of these sections revealed tha t both TNFalpha and IL-1 beta were associated with macrophages, partic ularly those in the synovium overlying cartilage (pannus) and endothel ial cells. Positive staining was seen at the CPJ in RA and in similarl y located tissue in OA. The similar distribution of cytokines in OA wa s unexpected even if the overall numbers of tissue and infiltrating ce lls in the CPJ were different in the two diseases. This highlights the possible role played by endogenous inhibitors [1, 2] in influencing t he degree of cytokine activity necessary to explain the different path ogenic mechanisms in RA and OA.